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*
Institute for Brain and Immune Disorders, Minneapolis Medical Research Foundation, Minneapolis, MN 55404; and
College of Veterinary Medicine and
Medical School, University of Minnesota, Minneapolis, MN 55404
Understanding the influence of immune effector mechanisms on CMV
infection of the CNS may facilitate the development of immunotherapies
for viral encephalitis. Using cultures of highly purified, fully
permissive primary human astrocytes, proinflammatory cytokines, but not
antiinflammatory cytokines or 
-chemokines, were found to inhibit CMV
expression, DNA synthesis, and replication. Treatment with certain
proinflammatory cytokines 24 h before CMV infection markedly
suppressed viral expression in astrocytes. TNF-
, IL-1, and
IFN-
all inhibited CMV expression (70 ± 4.2%, 65 ±
3.4%, and 82 ± 3.6% inhibition of viral expression,
respectively, n = 5). In contrast, no viral
suppression was observed following IL-6 treatment. Suppressive activity
was dependent on the addition of cytokines before CMV infection.
Cytokine pretreatment did not affect CMV entry into primary astrocytes,
and the observed cytokine-induced suppressive activity was not affected
by the NO synthase inhibitor
NG-monomethyl-L-arginine
(NGMA). Instead, the suppressive effect appeared to be
mediated through a mechanism involving inhibition of CMV major
immediate early promoter activity. These results support the hypothesis
that proinflammatory cytokines possess anti-CMV activity in brain
cells and may lead to new interventions for CMV encephalitis based upon
immunotherapy.
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